Current management: Management of rheumatic diseases in the era of biological anti-rheumatic drugs.

Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.
Acta Orthopaedica (Impact Factor: 2.74). 11/2005; 76(5):614-9. DOI: 10.1080/17453670510041673
Source: PubMed
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    ABSTRACT: The treatment of rheumatic diseases has been the focus of many clinical studies aiming to achieve the best combination of drugs for symptom reduction. Although improved understanding of the pathophysiology of rheumatic diseases has led to the identification of effective therapeutic strategies, its cure remains unknown. Biological agents are a breakthrough in the treatment of these diseases. They proved to be more effective than the other conventional therapies in refractory inflammatory rheumatic diseases. Among them, tumor necrosis factor inhibitors are widely used, namely Etanercept, Infliximab, or Adalimumab, alone or in combination with disease-modifying antirheumatic drugs. Nevertheless, severe adverse effects have been detected in patients with history of recurrent infections, including cardiac failure or malignancy. Currently, most of the available therapies for rheumatic diseases do not have sufficient tissue specificity. Consequently, high drug doses must be administrated systemically, leading to adverse side effects associated with its possible toxicity. Drug delivery systems, by its targeted nature, are excellent solutions to overcome this problem. In this review, we will describe the state-of-the-art in clinical studies on the treatment of rheumatic diseases, emphasizing the use of biological agents and target drug delivery systems. Some alternative novel strategies of regenerative medicine and its implications for rheumatic diseases will also be discussed.
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    ABSTRACT: Tumor necrosis factor-alpha (TNF-alpha) is a key mediator of inflammatory diseases, including rheumatoid arthritis (RA), and anti-TNF-alpha drugs such as etanercept are effective treatments. Splice-switching oligonucleotides (SSOs) are a new class of drugs designed to induce therapeutically favorable splice variants of targeted genes. In this work, we used locked nucleic acid (LNA)-based SSOs to modulate splicing of TNF receptor 2 (TNFR2) pre-mRNA. The SSO induced skipping of TNFR2 exon 7, which codes the transmembrane domain (TM), switching endogenous expression from the membrane-bound, functional form to a soluble, secreted form (Delta7TNFR2). This decoy receptor protein accumulated in the circulation of treated mice, antagonized TNF-alpha, and altered disease in two mouse models: TNF-alpha-induced hepatitis and collagen-induced arthritis (CIA). This is the first report of upregulation of the endogenous, circulating TNF-alpha antagonist by oligonucleotide-induced splicing modulation.
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    Acta Orthopaedica 12/2010; 81(6):660-6. · 2.74 Impact Factor

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Aug 13, 2014